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Here is a thorough guide to ECG patterns in MI and ischemia, drawn from Harrison's 22E, Tintinalli's Emergency Medicine, and Goldman-Cecil Medicine.
ECG in Myocardial Infarction and Ischemia
The Physiology Behind the Findings
Ischemia lowers the resting membrane potential and shortens action potential duration, creating a current of injury between normal and ischemic zones. This is what shifts the ST segment on the surface ECG.
- Subendocardial ischemia - ST vector shifts toward the inner cavity → leads overlying the area show ST depression (with reciprocal ST elevation in aVR)
- Transmural (epicardial) injury - ST vector shifts outward → overlying leads show ST elevation
STEMI vs NSTEMI - Key Distinction
| Feature | STEMI | NSTEMI |
|---|---|---|
| ST changes | ST elevation meeting criteria | ST depression / T-wave changes / no changes |
| Troponin | Elevated | Elevated |
| Reperfusion urgency | Immediate (cath lab activation) | Guided by risk stratification |
| Mechanism | Complete occlusion (usually) | Partial occlusion / demand ischemia |
The distinction matters because emergency reperfusion (primary PCI or thrombolysis) is consistently effective for STEMI, while the indication in NSTEMI depends on ongoing risk assessment. - Harrison's 22E
STEMI: Diagnostic ECG Criteria by Location
(From Tintinalli's Emergency Medicine)
| Territory | Leads with ST Elevation | Artery |
|---|---|---|
| Anteroseptal | V1, V2 (± V3) | Proximal LAD |
| Anterior | V1 - V4 | LAD |
| Anterolateral | V1 - V6, I, aVL | Proximal LAD |
| Lateral | I, aVL | Diagonal / LCx |
| Inferior | II, III, aVF | RCA (80%) or LCx (20%) |
| Inferolateral | II, III, aVF + V5, V6 | LCx |
| True posterior | Tall R in V1-V2 (R/S ≥ 1, R > 0.04 s); ST elevation on posterior leads V7-V9 | LCx or RCA |
| Right ventricular | II, III, aVF + ST elevation in right-sided leads (V3R-V6R) | Proximal RCA |
Standard numeric thresholds:
- ≥ 1 mm ST elevation in 2 contiguous limb leads
- ≥ 2 mm in 2 contiguous precordial leads (≥ 2.5 mm in men < 40 yrs; ≥ 1.5 mm in women in V2-V3)
Localizing the Culprit Artery
Inferior STEMI:
- ST elevation in III > II, with ST depression >1 mm in I and aVL → RCA
- Above findings + ST elevation in V1 or V4R → Proximal RCA (with RV involvement)
- ST elevation in I, aVL, V5-V6 with isoelectric/elevated ST in I → Left Circumflex (LCx)
- ST elevation aVR > V1 → Left main or proximal LAD
Right Ventricular Infarction:
Always obtain right-sided leads (V3R-V6R) in inferior STEMI to detect RV involvement. RV infarction has higher morbidity than isolated inferior infarction.
Temporal Evolution of STEMI
| Phase | ECG Findings |
|---|---|
| Earliest (minutes) | Hyperacute T waves - tall, peaked, broad |
| Early (hours) | ST elevation - upward-sloping ("tombstone"), ± loss of R wave |
| Established | Q waves develop (necrosis), ST begins to settle |
| Days to weeks | T-wave inversions in affected leads |
| Chronic | Q waves persist; T waves may normalize over months |
After Q-wave infarction, persistent ST elevation weeks later correlates with a severe wall motion disorder (possible ventricular aneurysm), not acute re-injury.
Q Waves
- A Q wave is abnormal if it is > 40 ms wide or > 25% of the R-wave amplitude in the same lead
- Q waves indicate myocardial necrosis sufficient to lose depolarization forces
- Old teaching: Q waves = transmural MI; no Q waves = subendocardial. This is no longer reliable - transmural infarcts can occur without Q waves, and subendocardial infarcts can produce Q waves
- Classify instead as Q-wave MI vs non-Q-wave MI
Reciprocal Changes
Reciprocal ST depression (in leads opposite the infarct zone) indicates:
- Larger area of injury at risk
- More severe underlying CAD
- Higher likelihood of pump failure and cardiovascular complications
- Increased mortality
In general, more ST segments elevated = more extensive injury.
Ischemia Patterns Without Complete Occlusion (NSTEMI / Unstable Angina)
Wellens' Syndrome (critical LAD stenosis)
Deep, symmetric T-wave inversions in V1-V4 (and sometimes I, aVL) indicate critical proximal LAD stenosis (Wellens' sign). ~75% have deeply inverted T waves; ~25% have biphasic T waves in the same leads. The T-wave changes appear when the patient is pain-free and may normalize when pain recurs - serial ECGs and pain correlation are key. This is a high-risk pattern requiring urgent catheterization.
Important ECG Limitations
- A single normal ECG does not exclude MI - a normal tracing throughout the entire course is uncommon but does occur
- LBBB, ventricular pacemaker rhythms, and WPW can all mask ischemic changes
- New (or presumed new) LBBB in the setting of chest pain - Sgarbossa criteria help identify superimposed STEMI:
- Concordant ST elevation ≥ 1 mm in any lead (concordant with QRS direction)
- Concordant ST depression ≥ 1 mm in V1-V3
- Excessive discordant ST elevation ≥ 5 mm (less specific)
- Note: <10% of patients with new LBBB actually have AMI
Summary: Quick Reference
| Finding | Interpretation |
|---|---|
| ST elevation in contiguous leads | STEMI - transmural injury |
| ST depression | Subendocardial ischemia / NSTEMI |
| Hyperacute T waves | Earliest STEMI - pre-elevation phase |
| Deep T inversions V1-V4 | Wellens' - critical LAD stenosis |
| Tall R in V1-V2 + ST depression V1-V3 | Posterior MI (mirror image) |
| ST elevation V3R-V6R | RV infarction |
| New Q waves | Established necrosis |
| Persistent ST elevation weeks post-MI | Wall motion disorder / ventricular aneurysm |
Sources: Harrison's Principles of Internal Medicine 22E (2025), Tintinalli's Emergency Medicine, Goldman-Cecil Medicine
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